Various types of pacing leads have been developed for endocardial introduction into different chambers of a patient's heart, typically a right ventricle, right atrial appendage, or coronary sinus. These flexible leads are usually constructed having an outer polymeric sheath encasing one or more electrical conductors. The conductors may be arranged coaxially or co-linearly and are insulated from one another. A distal end of each conductor is coupled to one or more electrodes while a proximal end of each conductor is coupled to a contact of a connector that is in turn coupled to an implantable pulse generator (IPG). The distal end of the lead is implanted to be positioned within the heart so that the electrodes may deliver pacing therapy by both sensing electrical activity of the heart muscle and stimulating the heart muscle.
The IPG may be a single chamber atrial pacemaker, a single chamber ventricular pacemaker, or a dual chamber pacemaker. The leads sense electrical activity in the heart and deliver stimulation pulses from the IPG when spontaneous electrical activity ceases, accelerates, or becomes disorganized. In the conventional single chamber atrial system, pacing therapy is delivered from lead electrodes located in the right atrial appendage. In the conventional single chamber ventricular system, pacing therapy is delivered from lead electrodes located in the right ventricular (RV) apex. In a conventional dual chamber system, leads function in both the right atrium and right ventricle. A lead implanted in the right atrium can provide pacing therapy to preserve both atrial-ventricular synchronization and the normal ventricular activation and contraction patterns. However, pacing from the atrial appendage is ineffective if the conduction between the atria and ventricles is blocked.
Automatic electrical impulses from the sinoatrial (SA) node, located in the anterosuperior wall of the right atrium, travel through the walls of the right and left atria to the atrioventricular (AV) node. At the AV node, the electrical impulse is delayed to allow time for the atria to complete their contraction before the ventricles are activated. The delay allows the ventricles to adequately fill with blood prior to contraction. The AV node is located in the septal wall of the right atrium immediately posterior to the tricuspid valve. After passing through the AV node, the impulse travels rapidly through the atrioventricular bundle, also known as the bundle of His, and spreads down the interventricular septum, visa the right and left bundle branches, and then throughout the walls of the ventricles, via the Purkinje fibers. The bundle of His extends from the AV node within the fibrous tissue between the tricuspid and mitral valves, where the atrioventricular septum joins the interventricular septum, and into the interventricular septum. Localized ischemia, inflammation, congenital defects, or compression of the AV node or the bundle of His can cause a block of electrical conduction between the atria and ventricles. Permanent block may also be caused by ablation to prevent conduction as a treatment for atrial fibrillation in some patients. Ventricular pacing is the standard means employed to bypass the block between the atria and ventricles.
Ventricular pacing is typically delivered from a lead's electrodes implanted in the apex of the right ventricle. Stimulation from this site is counter to the heart's natural operation. When the electrodes, located in the apex, deliver the electrical pulse the myocardial cells local to the apex begin to contract. The electrical signal then expands, relatively slowly compared to the heart's natural contraction, upward and outward until the ventricles fully contract. Therefore, ventricular pacing sends an electrical impulse that moves from the bottom to the top of the ventricles, and from the right to the left ventricle, causing an unnatural ventricular contraction pattern.
Some studies have put forth the proposition that significant problems are associated with pacing from the ventricular apex. It has been speculated that physiological pacing can cause ventricular wall abnormalities, inferior localized myocardial perfusion defects and mitral regurgitation. In addition, pacing from the ventricular apex has been alleged to create myofibrilar disarray and fatty deposits throughout the ventricles. Myofibrilar disarray and fatty deposits have been associated with congestive heart failure.
Therefore, what is needed is a method and apparatus for providing physiological pacing. Physiological pacing is defined herein as stimulation of the intrinsic conduction system of the heart that preserves a natural contraction pattern of the heart.